I was looking around pubmed for the effects of fasting on homocysteine concentration. I'd seen a reference which claimed that HCy rose progressively with extended fasting beyond 12h, making a 12h fast the ideal time to measure. For some reason (probably to do with having 10 windows open in two web browsers) I lost it. While pubmeding to relocate it (and failing) I tripped over this rather nice paper on starvation.
It looks very like the second author is the chap in the box and this news report gives an idea of how the first and second authors interacted. It also explains why there were no "pre box" blood values for Blaine!
The paper has a number of gem lines in it. First was that, whatever homocysteine levels do in acute starvation, by 44 days of water fasting they are normal. Normal does not appear to be zero.
Next was the acute hypophosphataemia induced by re feeding. This kicked in by the end of day one. By this time Blaine had been given three cartons of a commercial liquid "food" including a total of just under 40 grams of sucrose. I wouldn't like to mention fructose as a trigger for hypophosphataemia, but it does get an honourable mention here and we've all listened to Lustig discuss fructose the net. Glucose also requires its place in the syndrome too. Dr Powel-Tuck seems to feel that this hypophosphataemia is to do with the energy intake. I suppose this is true if you are stuck in the time warp that energy=glucose, before anyone realised that free fatty acids could be used for energy. As far as I am aware no one has ever precipitated acute hypophosphataemia with an Intralipid infusion, disgusting though the thought of soya bean oil intravenously might be.
You just have to wonder what a supply of calories as fat and protein might have done by perhaps using, gasp, cheese. High in phosphate anyway.... Then add that essential nutrient, sucrose, later. In fact on day five Blaine took himself to the hospital canteen and had fish and chips against doctors orders. Marked fluid retention was the end result but nothing worse.
The fluid retention is very interesting. This is what they noted:
"A raised haematocrit on admission (reflecting haemoconcentration) changed to progressively lower values, despite cautious refeeding, and total avoidance of saline or additional salt during the hospital stay (Table 3). Albumin concentration on admission to hospital was slightly raised and declined gradually over 5 days probably due to plasma expansion. By day 10, 5 days after he left hospital on a free diet, he demonstrated mild pitting oedema."
and here is my favourite
"As refeeding raises plasma insulin, [then] potassium, phosphate and magnesium are driven intracellularly, and sodium extracellularly, expanding circulating volume and causing haemodilution, as indicated in D B by changes in his haematocrit and albumin levels."
It doesn't mention that insulin also causes renal sodium retention, but it does. I rather like this paper, I've not worked through the free full text but I note from the abstract that an insulin infusion with normoglycaemia causes sodium retention even in control rats, never mind spontaneously hypertensive rats. You learn so much from the control groups, even if thay are only rats. And we all thought that folks with hypertension while hyperinsulinaemic on a high carbohydrate diet were born with an in-built frusemide deficiency! Sounds more like Fanta poisoning to me. So, for Blaine, you have to ask whether the immediate return to a "balanced" diet, rich in nourishing sucrose and insulin spiking starch, is what precipitated the fluid retention and whether a more lipid based diet with gradual transition at real food for a few days before diving in to the "sugar as the main course with spuds for dessert" regime might have been less problematic.
I can't imagine anyone testing this idea, so perhaps it's a good job we have phosphate infusions available in UK teaching hospitals to pull post-starvation patients back from the brink of iatrogenic sugar poisoning during refeeding!